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3 publications mentioning hsa-mir-1468

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-1468. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 386
Other miRNAs from this paper: mmu-mir-130b, hsa-mir-130b, hsa-mir-1469
Overexpression of miR-1468 promoted cell proliferation (b, c), colony formation (d), cell cycle progression (e) and inhibited apoptosis (f) in Hep3B cells, while down-regulation of miR-1468 inhibited cell proliferation (b, c), colony formation (d), cell cycle progression (e) and promoted apoptosis (f) in MHCC-97 L cells. [score:10]
a and b The expression of CITED2 and UPF1 in miR-1468 high -expressing tumors was significantly lower than that in miR-1468 low -expressing tumors, as determined by qRT-PCR and immunoblotting. [score:7]
Furthermore, miR-1468 overexpression significantly inhibited the mRNA and protein expression of CITED2 and UPF1 in Hep3B cells (P < 0.05, respectively, Fig. 4c, d). [score:7]
Consistently, CITED2 and UPF1 protein expression in miR-1468 high -expressing tumors were obviously lower than those in miR-1468 low -expressing tumors as suggested by IHC, and both CITED2 and UPF2 staining were weaker than adjacent nontumor tissues (P < 0.05, Fig. 5d). [score:7]
These results reveal that miR-1468 inhibits CITED2 and UPF1 expression by directly binding to their 3’-UTR. [score:6]
Furthermore, CITED2 and UPF1 were down-regulated in HCC tissues, and modulating their expression could reverse the biological function of miR-1468 in HCC cells. [score:6]
Moreover, CITED2 or UPF1 knockdown abolished the inhibitory effects of miR-1468 inhibition on HCC cells (P < 0.05, Fig. 6b-f). [score:6]
The tumor growth curves revealed that miR-1468 overexpression significantly promoted the tumor growth, while miR-1468 knockdown inhibited the tumor growth of HCC cells in mice (P < 0.05, Fig.   3a). [score:6]
d miR-1468 overexpression reduced the expression of CITED2 and UPF1 protein in Hep3B cells and miR-1468 knockdown increased the level of CITED2 and UPF1 protein in MHCC-97 L cells. [score:6]
showed that miR-1468 overexpression inhibited, while miR-1469 knockdown increased the luciferase activity of wild-type (wt) CITED2 or UPF1 3’-UTR but not the mutant (mt) CITED2 or UPF1 3’-UTR (P < 0.05, Fig. 4b). [score:6]
Furthermore, we confirmed that miR-1468 inhibited PPAR-γ/AKT signaling activity through directly suppression of Cbp/p300 interacting transactivator with Glu/Asp rich carboxy-terminal domain 2 (CITED2) and Up-frameshift protein 1 (UPF1). [score:6]
In addition, immunoblotting analysis confirmed that up-regulated miR-1468 level obviously increased Cyclin D1 and Bcl-2 expression, while reduced the levels of p21 and Bax (P < 0.05, respectively, Fig. 2g). [score:6]
Tumor growth curve revealed that miR-1468 overexpression significantly promoted, while miR-1468 knockdown inhibited tumor growth in vivo. [score:6]
Furthermore, we confirm that miR-1468 promotes cell proliferation, colony formation, cell cycle progression and inhibits apoptosis by directly targeting CITED2 and UPF1 mediated PPAR-γ/AKT pathway. [score:6]
As shown in Fig.   7a, overexpression of miR-1468 significantly inhibited, while miR-1468 knockdown promoted PPAR-γ/AKT pathway in HCC cells (P < 0.05, Fig. 7a), with change of p-AKT level rather than total AKT (P < 0.05, Fig. 7a). [score:6]
Here, we demonstrated that miR-1468 expression was up-regulated in HCC tissues and cell lines. [score:6]
b miR-1468 overexpression significantly suppressed, while miR-1468 loss increased the luciferase activity that carried wild-type (wt) but not mutant (mt) 3’-UTR of CITED2 or UPF1. [score:5]
HCC patients with higher expression of miR-1468 had worse overall survival (c) and disease-free survival (d). [score:5]
a miR-1468 -overexpressing Hep3B cells that were transfected with empty vector (EV) or CITED2, UPF1 overexpression plasmid were subjected to western blot for CITED2 and UPF1. [score:5]
Jiang et al. confirmed that miR-1468 inhibited cell proliferation and induced cell cycle arrest by targeting ribonucleotide reductase large subunit M1 (RRM1) in glioma [12]. [score:5]
d Representative immunohistochemical staining showed a weak staining of CITED2, UPF1 in miR-1468 high -expressing HCC tissue and strong staining of CITED2, UPF1 in the miR-1468 low -expressing tumor. [score:5]
c Hep3B and MHCC-97 L cells that were transfected with precursor miR-1468 and miR-1468 inhibitors (anti-miR-1468), respectively, were subjected to qRT-PCR for CITED2 and UPF1 mRNA expression. [score:5]
PPAR-γ agonist rosiglitazone treatment inhibited the promotive effects on cell proliferation (b, c), colony formation (d), cell cycle progression (e) and apoptosis (f) of miR-1468 overexpressing Hep3B cells. [score:5]
CITED2 or UPF1 knockdown reversed the suppressive effects of miR-1468 knockdown in MHCC-97 L cells (b- f). [score:5]
As measured by qRT-PCR, we confirmed that miR-1468 was effectively upregulated in Hep3B or downregulated in MHCC-97 L cells (P < 0.05, Fig.   2a). [score:5]
Previous study reported that miR-1468 showed an up-regulated tendency and might be a potential prognostic biomarker in HCC samples derived from TCGA database. [score:4]
f Xenografts tissues immunohistochemical staining of CITED2 and UPF1 in miR-1468 overexpression or knockdown subcutaneous tumor nodules. [score:4]
Moreover, CITED2 and UPF1 were identified as direct downstream targets of miR-1468 in HCC cells, and mediated the functional effects of miR-1468 in HCC, resulting in peroxisome proliferator-activated receptor-γ (PPAR-γ)/AKT signaling activation. [score:4]
Conversely, T0070907 (50 μM), an antagonist of PPAR-γ, rescued the effects of miR-1468 knockdown on biological function of HCC (P < 0.05, Fig. 7b-f) in miR-1468-suppressive MHCC-97 L cells. [score:4]
CITED2 or UPF1 knockdown mimics effects of miR-1468 overexpression in MHCC-97 L cells (B-F). [score:4]
Our data reveal a novel role for miR-1468 in HCC development and progression, and suggest miR-1468 as a potential target for HCC diagnosis and treatment. [score:4]
Previous study reported that miR-1468 showed an up-regulated tendency and might be a potential prognostic biomarker in HCC samples derived from The Cancer Genome Atlas (TCGA) database [16]. [score:4]
Fig. 4CITED2 and UPF1 are direct targets of miR-1468 in HCC cells. [score:4]
PPAR-γ antagonist, T0070907, reversed the suppressive effects of miR-1468 knockdown in MHCC-97 L cells. [score:4]
By contrast, the expression of CITED2 and UPF1 were significantly increased by miR-1468 knockdown in MHCC-97 L cells (P < 0.05, respectively, Fig. 4c, d). [score:4]
miR-1468 is up-regulated in HCC and correlates with patients’ survival. [score:4]
In clinical samples of HCC, miR-1468 inversely correlated with the levels of CITED2 and UPF1, which were confirmed to be down-regulated in HCC. [score:4]
In present study, we confirmed that miR-1468 was up-regulated in HCC tissues and cell lines, which was consistent with TCGA data. [score:4]
In accordance, miR-1468 knockdown inhibited the growth and induced apoptosis of MHCC-97 L cells (P < 0.05, Fig. 2b-g). [score:4]
However, miR-1468 knockdown inhibited proliferation and induced apoptosis in vivo (P < 0.05, Fig. 3b, c). [score:4]
Representative immunostaining and TUNEL assays revealed that miR-1468 overexpression significantly increased the number of Ki-67 positive cells and inhibited the number of apoptotic cells. [score:4]
We further evaluated the expression of CITED2 and UPF1 in xenografted tissues and found that miR-1468 overexpression group showed a weak CITED2 and UPF1 staining, however, miR-1468 knockdown group showed opposite effects (P < 0.05, Fig. 5f). [score:4]
g of cycle regulator Cyclin D1 and p21, apoptosis-related protein Bcl2/Bax expression in the presence and absence of miR-1468. [score:4]
Our study considers miR-1468 as a potential diagnostic marker and therapeutic target for HCC. [score:3]
We found that miR-1468 was significantly up-regulated in HCC tissues compared with matched non-tumor tissues (P < 0.05, Fig.   1a). [score:3]
CITED2 or UPF1 restoration abrogated the effects of miR-1468 overexpression on cell proliferation (b, c), colony formation (d), cell cycle progression (e) and apoptosis (f) of Hep3B cells. [score:3]
a Hep3B and MHCC-97 L cells that were transfected with corresponding miRNA vectors were subjected to qRT-PCR for miR-1468 expression. [score:3]
Taken together, this research supports the first evidence that miR-1468 plays an oncogenic role in HCC via activating PPAR-γ/AKT pathway by targeting CITED2 and UPF1, and represents a promising therapeutic strategy for HCC patients. [score:3]
AKT inhibitor MK2206, or AKT phosphorylation activator IGF-1, abolished the cell proliferation (a, b), colony formation (c), cell cycle progression (d) and apoptosis (e) of HCC cells which were transduced of miR-1468 vectors. [score:3]
To explore the expression level of miR-1468 in HCC, we performed qRT-PCR to measure its expression in 40 pairs of randomly selected tumor tissues and matched adjacent non-tumor tissues. [score:3]
In addition, alteration of CITED2 or UPF1 expression also abolished the effects of miR-1468 on cell cycle and apoptosis-related protein (P < 0.05, Fig. 6g). [score:3]
In summary, we demonstrate that miR-1468 overexpression acts as an independent biomarker for indicating poor prognosis of HCC patients. [score:3]
Previous study reveals that the target genes of miR-1468 are enriched in PPAR signaling pathway [16]. [score:3]
In present research, we demonstrated that miR-1468 overexpression was associated with poor prognostic features and reduced survival of HCC patients. [score:3]
Furthermore, Kaplan-Meier analysis revealed that HCC patients with high miR-1468 level showed a significant shorter overall survival (P = 0.0004, Fig. 1c) and disease-free survival (P = 0.0006, Fig. 1d). [score:3]
In this study, we demonstrated that miR-1468 promoted cell proliferation, cell cycle progression, colony formation and inhibited apoptosis by gain- and loss-of function experiment in vitro and in vivo. [score:3]
In addition, AKT phosphorylation activator, IGF-1, increased cell proliferation, cell cycle progression, colony formation and inhibited apoptosis (P < 0.05, respectively, Fig. 8a-e) in MHCC-97 L-anti-miR-1468 cells. [score:3]
In addition, miR-1468 was an independent factor for predicting 5-year overall and disease-free survival in HCC patients (P = 0.003 and 0.007, respectively, Table  2). [score:3]
Restoration of CITED2 or UPF1 expression at least partially abolished the biological effects of miR-1468 on HCC cells. [score:3]
As expected, miR-1468 overexpression increased the number of Ki67 positive staining cells and reduced the number of apoptotic cells (P < 0.05, Fig. 3b, c). [score:3]
Inactivation of AKT phosphorylation by MK2206 in miR-1468 -overexpressing Hep3B cells significantly decreased cell proliferation, cell cycle progression, colony formation (P < 0.05, Fig.   8a-d) and induced apoptosis (P < 0.05, Fig. 8e). [score:3]
First, miR-1468 negatively modulated CITED2 and UPF1 expression in HCC cells. [score:3]
Third, miR-1468 was inversely correlated with the expression of CITED2 and UPF1 in HCC tissues. [score:3]
To confirm that AKT phosphorylation contributes to the biological function of miR-1468 in HCC cells, we used AKT inhibitor MK2206 or AKT activator IGF-1 (insulin-like growth factor 1) to alter AKT activation. [score:3]
miR-1468 promotes cell growth and inhibits apoptosis of HCC cells. [score:3]
In lung adenocarcinoma, miR-1468 expression was significantly correlated with recurrence-free survival [14]. [score:3]
miR-1468 inversely correlates with CITED2 and UPF1 expression in HCC tissues. [score:3]
Taken together, these data suggest that CITED2 and UPF1 expression are inversely associated with miR-1468 in HCC tissues. [score:3]
We found that rosiglitazone at least partially inhibited miR-1468 -induced cell proliferation, cell cycle progression, colony formation and apoptosis resistant in HCC cells (P < 0.05, Fig. 7b-f). [score:3]
Moreover, we provided the first evidence that the target genes of miR-1468 were CITED2 and UPF1. [score:3]
miR-1468-suppressive MHCC-97 L cells that were transfected with scrambled siRNA or CITED2, UPF1 siRNA were subjected to western blot for CITED2, UPF1. [score:3]
To conclude, our data offer the promising evidence that miR-1468 overexpression acts as an independent risk factor for indicating poor prognosis of HCC patients. [score:3]
Moreover, inhibition of CITED2 or UPF1 mimics miR-1468 -induced effects in control cells (Additional file  1: Figure S1). [score:3]
Moreover, we found that the mRNA level of CITED2 and UPF1 was inversely correlated with miR-1468 expression in the HCC tissues (R [2] = 0.5753 and 0.5636, P < 0.0001, Fig. 5c). [score:3]
Comparing differences in the expression of miR-1468 between (a) HCC and matched tumor-adjacent tissues and (b) HCC cell lines and the immortalized hepatic cell line LO2. [score:3]
Fig. 5An inverse correlation between miR-1468 and CITED2, UPF1 expression is observed in HCC tissues. [score:3]
Therefore, our results confirm that miR-1468 exerts a critical role in HCC progression and represents a potential target for HCC diagnosis and treatment. [score:3]
CITED2 and UPF1 are downstream targets of miR-1468 in HCC. [score:3]
As determined by flow cytometry, overexpression of miR-1468 promoted cell cycle transition from G1 to S phase (P < 0.05, Fig. 2e) and apoptosis resistance (P < 0.05, Fig. 2f). [score:3]
CITED2 or UPF1 restoration mimics the effects of miR-1468 knockdown on cell proliferation (B, C), colony formation (D), cell cycle progression (E) and apoptosis (F) of Hep3B cells. [score:2]
More significantly, CITED2 and UPF1 -mediated PPAR-γ/AKT pathway may be directly implicated in the oncogenic function of miR-1468 in HCC. [score:2]
The colony formation assay revealed that ectopic expression of miR-1468 significantly increased cell colonies (P < 0.05, Fig. 2d). [score:2]
However, the percentage of Ki-67 positive cells in tumors arising from the miR-1468 knockdown group was significantly lower and the percentage of apoptotic cells was significantly higher than that in the negative control (NC) group. [score:2]
Thus, these data demonstrate that miR-1468 regulates HCC cell proliferation, cell cycle progression, colony formation and apoptosis in vitro. [score:2]
CCK8 and EdU proliferation assays found that miR-1468 overexpression enhanced cell proliferation (P < 0.05, Fig. 2b, c). [score:2]
Hep3B (5 × 10 [6]) cells that were transfected with miR-1468 or miR-control vectors or MHCC-97 L cells with anti-miR-1468 were mixed in 150 μl of Matrigel and were inoculated subcutaneously into the flank of nude mice. [score:1]
Here, AKT phosphorylation was critical for the biological effects of miR-1468 in HCC. [score:1]
Moreover, increased miR-1468 level was obviously correlated with malignant clinicopathological features, including large tumor size, high histological grade and advanced tumor stage. [score:1]
f indicated that modulating AKT phosphorylation reversed the effects of miR-1468 alteration on cell cycle and apoptosis associated factors of HCC cells. [score:1]
In this study, alteration of PPAR-γ activation could abolish the effects of miR-1468 on HCC growth. [score:1]
Our data indicates that miR-1468 may server as a novel predictive biomarker for HCC patients. [score:1]
e, f Immunofluorescence staining of CITED2 and UPF1 after transduction of miR-1468. [score:1]
MiR-1468, a novel cancer related microRNA, was dysregulated and could predict patients’ survival in diverse cancers [11]. [score:1]
miR-1468 facilitates HCC cell proliferation and cell cycle progression, and induces apoptosis in vitro and in vivo. [score:1]
CITED2 or UPF1 restoration reversed the promotive effects of miR-1468 on cell proliferation (P < 0.05, Fig. 6b, c), colony formation (P < 0.05, Fig. 6d), cell cycle progression (P < 0.05, Fig. 6e) and apoptosis (P < 0.05, Fig. 6f). [score:1]
These data suggest that miR-1468 is involved in HCC progression and represents as a promising biomarker for HCC therapy. [score:1]
Taken together, we confirm that miR-1468 promotes HCC cell growth by modulation of PPAR-γ/AKT signaling (Additional file  3: Figure S3). [score:1]
Moreover, alteration of PPAR-γ or AKT phosphorylation could reverse the function of miR-1468 in HCC. [score:1]
To investigate whether PPAR-γ mediated miR-1468 -induced biological function in HCC cells, we treated miR-1468 -overexpressing Hep3B cells with the agonist rosiglitazone (40 μM). [score:1]
Nevertheless, the function of miR-1468 and its underlying molecular mechanisms in HCC remain unknown. [score:1]
Fig. 8AKT phosphorylation is essential for the biological function of miR-1468 in HCC. [score:1]
Moreover, miR-1468 was decreased in blood -based microRNA biomarker in early diagnosis of pancreatic cancer [15]. [score:1]
Fig. 7PPAR-γ/AKT signaling is essential for the biological function of miR-1468 in HCC. [score:1]
g Alteration of CITED2 or UPF1 abolished the effects of miR-1468 on cell cycle and apoptosis associated factors. [score:1]
PPAR-γ/AKT signaling is essential for the biological function of miR-1468 in HCC. [score:1]
Fig. 6Modulation of CITED2 or UPF1 partially abolishes miR-1468 -mediated cellular processes in HCC. [score:1]
These results confirm that CITED2 and UPF1 are functional mediators of miR-1468 in HCC cells. [score:1]
g indicated that modulating PPAR-γ activation reversed the effects of miR-1468 alteration on cell cycle and apoptosis associated factors of HCC cells. [score:1]
Second, miR-1468 affected the luciferase activity of wt 3’UTR but not mt 3’UTR of CITED2 and UPF1. [score:1]
In papillary renal cell carcinoma (pRCC), miR-1468 was significantly associated with patient survival and identified by multivariate Cox regression analyses as potential independent prognostic factors in pRCC [13]. [score:1]
Modulation of CITED2 or UPF1 mimics miR-1468 -induced cellular processes in HCC. [score:1]
miR-1468 Hepatocellular carcinoma CITED2 UPF2 PPAR-γ Tumor growth Hepatocellular carcinoma (HCC) is the fifth most common malignancies worldwide and the second leading cause of cancer-related death which contribute to increasing morbidity and mortality in China according to world health organization (WHO) [1, 2]. [score:1]
The mutant binding site was generated in the complementary site for the seed region of miR-1468. [score:1]
Taken together, our results demonstrate that AKT phosphorylation exerts an important role in miR-1468 -mediated HCC grwoth. [score:1]
Clinical analysis revealed that increased miR-1468 level was significantly correlated with malignant prognostic features and shorter survival. [score:1]
Overview of miR-1468 -induced tumor progression and activates PPAR-γ -mediated AKT signaling in human hepatocellular carcinoma. [score:1]
a miR-1468 and its putative binding sequences in the 3’-UTR of CITED2 and UPF1. [score:1]
n. s, no significance, * P < 0.05 Next, we measured the expression of CITED2 and UPF1 in different miR-1468 groups. [score:1]
Taken together, these results demonstrate that miR-1468 promotes tumor growth of HCC in vitro and in vivo. [score:1]
AKT phosphorylation is critical for the biological effects of miR-1468 in HCC. [score:1]
Restoration of CITED2 and UPF1 reverses the biological effects of miR-1468 on HCC cells. [score:1]
Moreover, alternation of PPAR-γ also abolished the effects of miR-1468 on cell cycle and apoptosis-related proteins (P < 0.05, Fig. 7g). [score:1]
Next, we divided all HCC patients into miR-1468 high (n = 50) and low (n = 49) group according to median value. [score:1]
Our data revealed that both CITED2 and UPF1 levels in HCC tissues with high miR-1468 level were significantly lower than those in low miR-1468 group (P < 0.05, Fig.   5a, b). [score:1]
In conclusion, our results indicate that PPAR-γ/AKT signaling plays an essential role in miR-1468 -induced HCC growth. [score:1]
Gain- and loss-of-function experiments indicated that miR-1468 promoted cell proliferation, colony formation, cell cycle progression and induced apoptosis of HCC cells in vitro and in vivo. [score:1]
a Representative pictures of HCC xenografts from both Hep3B-miR-1468 (left panel) and MHCC-97 L-anti-miR-1468 cells (right panel). [score:1]
c An inverse correlation between the levels of miR-1468 and CITED2, UPF1 mRNA was observed in HCC tissues. [score:1]
Moreover, miR-1468 was an independent prognostic factor in predicting survival of HCC patients. [score:1]
As shown in Table 1, increased miR-1468 level was markedly associated with large tumor size (≥5 cm; P = 0.006), high histological grade (Edmondson-Steiner grade III + IV; P = 0.018) and advanced tumor stage (TNM stage III + IV; P = 0.014). [score:1]
The direct binding of miR-1468 to 3’UTR of Cbp/p300 interacting transactivator with Glu/Asp rich carboxy-terminal domain 2 (CITED2) and Up-frameshift protein 1 (UPF1) was confirmed by luciferase reporter assay. [score:1]
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2
[+] score: 25
Other miRNAs from this paper: hsa-mir-24-1, hsa-mir-24-2, hsa-mir-584
SNPs rs2662411 and rs1778335 might regulate mRNA expression of CMBL and PIP4K2A through influence on miRNA expression of hsa-miR-584 or hsa-miR-1468. [score:6]
Similarly, in LCLs SNP rs1778335 was associated with higher expression of hsa-miR-1468 (r-value = 0.194, p-value = 1.57 × 10 [-3]), which was associated with lower expression of PIP4K2A (r-value = −0.267, p-value = 8.24 × 10 [-3]); in SCLC cell line knockdown of PIP4K2A resulted in paclitaxel resistance; those results were consistent with the association of SNP rs1778335 with higher paclitaxel IC50 in LCLs (r-value = 0.248, p-value = 6.04 × 10 [-5]) and worse overall survival in SCLC patients (HR = 1.602, p-value = 0.019). [score:6]
Similarly, SNP rs1778335, close to gene PIP4K2A, was associated with the expression of hsa-miR-1468 with p-value = 1.57 × 10 [-3] (r-value = 0.194), and this microRNA was associated with mRNA expression of PIP4K2A with p-value = 8.24 × 10 [-3] (r-value = −0.267). [score:5]
Integrated SNP-miRNA-mRNA expression association analysis indicated that SNPs rs2662411 and rs1778335 were associated with mRNA expression of CMBL or PIP4K2A through hsa-miR-584 or hsa-miR-1468. [score:5]
SNPs rs2662411 and rs1778335 were associated with mRNA expression of CMBL or PIP4K2A through microRNA (miRNA) hsa-miR-584 or hsa-miR-1468. [score:3]
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3
[+] score: 2
The seven dysregulated miRNAs including hsa-miR-182-5p, hsa-miR-183-5p, hsa-miR-96-5p, hsa-miR-1271-5p, hsa-miR-182-3p, hsa-miR-1468-5p, and hsa-miR-135b-3p (Table S1 in file S1) were confirmed by the AUC of ROC curve (AUC = 0.965) with 97% sensitivity and 85% specificity (Figure S5 in file S1). [score:2]
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